Arterial blood gases made easy , SÁCH VỀ KHÍ MÁU ĐỘNG MẠCH DỄ HIỂU NHẤT

QUYỂN SÁCH TIẾNG ANH VỀ PHÂN TÍCH KHÍ MÁU ĐƠN GIẢN DỄ HIỂU NHẤT, PHÙ HỢP CHO SINH VIÊN, BÁC SĨ . PHÂN TÍCH KHÍ MÁU LÀ ĐIỀU BẮT BUỘC PHẢI BIẾT ĐỐI VỚI SINH VIÊN Y KHOA, BÁC SĨ, SÁCH MÔ TẢ NGẮN GỌN NHƯNG RẤT DỄ HIỂU VÀ DỄ DÀNG ỨNG DỤNG LÂM SÀNG, NÊU RÕ CƠ CHẾ VÀ TÌNH HUỐNG RÕ RÀNG, KHIẾN CHO VIỆC PHÂN TÍCH KHÍ MÁU TRỞ NÊN ĐƠN GIẢN NHẤT CÓ THỂ

lain A M Hennessey MBCha (Ho,n)'" IH='I M'eS

Senior House Officer, Ne()nol<lllnlens;lIe Core

Royol United HosPIIaI, Bath, UK

Alan G Ja pp MIlCh iHoNl SS< IHomI MlCP

Clinical Research Fellow in Cordiology

University 01 Edinburgh, UK

bLSEVlFR

LNTNGSTONE

CLSEVlER

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If you've taken the time to open Arfnwl Blood Gases Mnd, l-:tJsy, you must believe that artenal blood gases (AHtJi) are unportant but not

Pntirely:,lraightforward.

We ft>rtamly agn ~ on the first pomt: ABC analysis now play:. il/1

indispensablf' role in the assessment and manilKcmcnt of pahf'nh;wltll a huge range of acute moollal and surgu"al problems AccuratE'

ABG interpretation is undoubtedly a fundamental skill U1 modem

clink'" medianl::.

On the SI.'('ond pomt, we hope this book ran bto of a~sislance.

Throughout our aim~ have ~,\ to emphasi<:l' the key concept~,

fnrus on priKtical and useful aspects of ABG analysi!! and dvoid

extrant"Ous detal1 \Vc believe lThlny medical and nursing students, JWlior doctors and specmhst nurses will benefit from a dear, roncise

guide to performing thl? te<:hnl4uc and interpN>tmg the results

lain A M HeJUlCSSCY

Alan Glapp

•

1.7 When and why IS on ABG required? 48

1 1

INTRODUCTION

Arterial blOOl"l ~,\S (ABC) analysis ~fers 10 the mcasuremE'nt of pi I

and the partial pn:s~.m:s of oxygen (Oz) and carbon dioxide (Co,) in

artt>rial blood From these values we can ass s ttwo state of tJdJ buse

bolanCt in blood and how well lungs are ~riormingtheir job ofgll5

,:xc}Ul11gt.

Already the~ afC questions: what is meant by 'acid-base status'?

What is.:l 'partial pressure'? Why do they matter? It helps to break

things cJown

Part 1 of this book is designed to answer the:;e questions. We start with a few p<lg~ covering theb.1sic CSSli:Jlhals of respiratory and aad

base physIology: plel1St' do not skip them! Ifyou understand these COT@

concepts, thf' rest wlll follow seamles.s1y Part 1 abo t:xplainll how, when and why 10 obtain an ABC sample, bcforeconduding with a

'iimple step by-step guide to intcrpretin~ABG data

Part 2 tht-n allows you to put aU of this into practice with a senes

of case ~ariosinvolving ABG analysis You may already have a

method fOT interpreting ABGs but we lUge you to try our system (set NIt in section 1.9) that offers a logical, rndhodical and consistent way

of approachmg ABGs By sceinM: how this system can idt'Jltify all of

~ majOr patterns of ABG abnonnalities we hope you will gain thenecf"<i o;ary confidence to apply it in clinical practice.

3

PULMONARY GAS

EXCHANGE: THE BASICS

OUf ~lls use oxygpn (0,) to generate CJ\cq:;y and produce carbondioxide (COz) as waste Blood <;upphes cdb with the O2thfoy need

and dears the unwanted COt. This p~<; d~dson the ability of

our lungs to f'nnch blood with O:z and rid it of Co,

Pulmonary Ras rxcllatlg' ",fel'S to the ttdusfer of O:zfrom the

atmosphe~t~) the bloodstream (oxygenation) and CO2 born thpbloodstrp-am to the aunosphcl'c (C02e-limination)

TIle cxchan~elakl"S plal'"P between uny air sacs call1''d alvroll andblood \'t$scls called mpilfl1n~.Because~y carll haxe exlTf'melythin walls and rome into very d06E' conmct(theal\'coIar-capillarymembrane),Co, and O:z arc able to move (diffu~) betw~them(Figure1)

02and co,lranSlBr

occurs attheaM!dar

B capIafy l,lfl!OOrar,I

PULMONARY GAS EXCHANGE: THE BASICS

ABC.s help us to assess the ~ltectivencssofgas exchange by

providing measurernt"tlts of the partial pmiSurn of O2 and COz in

arterial blood - thE" PflOz.and Pa~.

Partial pressure dcscribe5 thE" contribution ofon~ individual gas

within a gas IJ\i.Jl.ture (such asair) to the total pre;sure When a gas

dissol\l~ m liquid (e.g blood), the amount dissolved depcnili; on thepartial pt'PllSUTe

Nole

~. partial pressure of 0 1

PalJl '" partial pre$5ure of O2in D.rl~ri.lblood

Gases move from areas ofhigherpartial pressure to lowE"I' partial

pICSSW\! Atthe alveolar-<apillary membrane, airin alveoli has a

higher 1\7 and lower Pro, than capillary blood Thus, OzmolecuJe:o;moVE" from alveoli lu blood and CO:z molecules move from blood toalveoli until the partial pressures arc equal

Co, mcJI,;~ up fV1l a til"/)' frodioil 01 air, so the pamol pressure of C~ in

in~,ed aIr IS negligible

•

f'Ut.MONARY GAS eXCHANGE; THE 8ASICS

CARlON DIOXIDE WM''''ATION

Diffusion of co,from lhe bluodstrPam to alveoli isso dficient that

COl elimination is actually limited by how quickly we can

"blow-off" the CO210 our alveoli Thus, the PilC02(which reflE'Cts the

overall amount ofC~ in arterial blood)is dttermined by al'Ot.'Olar

Drnhlahon - the total volume of air transported bctwt.:cnalveoli and

the outside world every minute

Vmtilation IAregulated byan area m the bralnstf>m called the

respiratory centre 'Thisarea containS specialised rca::ptun that sensethe PtlCOz and cvnnect with the muscles involved in breathing If

it isabnormal, the respiratorycentre adju~ts the rate and depth of

breathing acrordingIy (Figure 2)

Normally, hmgscanmaintAIn a normal P~eveninrondltioru;

whereCo,production i!'l unusually high(e.~ sepsIS). Consequently

an increased PIKOz (hypercapnia) always lD1plies reduced alveolar

ventilation

Key point

PaCo1 is controlled by vtnlil.llion ~ndthe level of v ntilation is

ildju5ted to m.aintilin PaCo1 within tight Iimils

•

•

I

PUlMONARY GAS EXCHANGE: THE BASICS

~Paco2" +V&nlilatioo

tPaC02" tVentla\loll

~ note on ••• hypoxic drive

In patients with chronicolfy high PoC02 levels (chronic hypercapnia), the

~iali-ed reo:;eptors thot deled CO2 kmlls can become de$ensilbed Thebody then relies on receptors that detect the POiJ-l to gouge the adequocy of

ventilation and low POOJ becomes the principal Vflnlilotory stimulus This is referred to as hypoxic drive.

In patientswho rely on h~ic drive, overzealous cOfrection of

hypoxoemio, with supplemental O:z, may depress ventilation, leading

to a colastrophlc riM in POCO:!. Patients with chronic hypercapnia

must therefore ~ given wpplementol O2 in a controlled fashion with

careful ABG monitoring. The same does not oppfy to potienb with ocut.

hypercapnia.

7

PULMONARY GAS EXCHANGE: THE BASICS

HAEMOG~O.'N OXYGEN SAtURATION (SO,)

Oxygenation is marc complicated than C~t'liminabon 1lte firstthing to realiSE' lS that the Po:!. does not actually teU llS how much

~ is inblood It only fTlf'asures free, unbound ~ moIecules- a tinyproportion of !he total

In fact, almost all0,.molecules inblood are bound to a protem called

hamwgfobin Hb (Pigure 3) Becau~ of!.his, the amount of O2 In blood

depends on two facton.:

capaCIty to carry.

2 Saturation of lib with 02 ($0,): this is the pcrccntaj.;c of

available bindin~sites on lib that ront3m an 02 molecule - i.e

how much of the carrying capacity is btrng used (Figure4).

Note

Soz:: O2 wtueation in (;my) blood

$Q:O:! "" O2 "tueation in Q:rlmal blood

It note on pulM ~it

So::>:2con be me<»ured using 0 Pfobe (pul!oe o imelerl opplied /Q the

finger or earlobe In most case$ it Pfovide$ odeqUQte informatioo 10

901.19-Q,ll,ygenarion, but it iller.s occurate witn saturatlon1 below 75% and

unre!iQble when plIfipherat perf",lion il poot Oximetry00e$ not provide

infoflTlOlion on f'acQ) w ~hwklllQr be u~ 0$ 0 wbditute for A8G onolyJis

In ventitololy impoir", l.

Key point

.Po,. is not a m('uu~ of the unount of O2in bJuod - ultimately theSaO:!;;md Hb concentration determine theD,.confent of arterialblood

•

PUlMONARY GAS EXCHANGE: THE BASICS

O:!tnnlklHb(M)

bo<md b hoomoglobin in blood.

HaemogIobil Fre9QIl)9lll Boln:I axygen 1TlOIea.M rnoIecUe ~ •

PUlMONARY GAS EXCHANGE: THE BASICS

OXYHAEMOGLOBIN DISSOCIATION CURVI

Vk now know that the amount of~in blood depenWi on the Hb

COTKt.>nlcationand the~.So what is the significance of the PQ:l?

Po;.can be thought ofIlS the driving force for O! molC'Cull.'$ to bind

to Hb: as such it regulates the Soz. Theoxyhapmoglobin dissociationCUC'Ye (Figure 5) showsthe So,.thai will result from any giV01 Po,

Ingenern, ~ higher the Paz, the highel" the Sov but Iht CUrtlt is not

littttlr. Tfw green line is known as the 'flat part of the cwve': changes

in ~ over this rangf' have relatively littleeffect on the50:1. In

contrast, the redline is known as the 'steep part of thf' curve': even

small c.hanges in PO].over this rangf" may have a major impacton~.

Note that, with a 'normal' PIlO:l of around 13 kPa (100mmHg), Hb is,more ocless, nUlximallystlhmdm (~>95%) This means blOl.X1 has

uwd up its D,-t:acryinK capacity and any further rise in Pao, willlWtsignificantly increase arterial D.z content

Key point

Po" is not the amount of O2 in blood but is the driving force for

5.lItunting Hb with 02"

I.

PUlMONARY GAS EXCHANGE: THE BASICS

Figuro S ~Jobjn disso:iotioIl anotl. The CUfVe defines the

,J.m.,,,sJ.ip beMun Po, and thepercfflJloGe so1uI"ation 01 haemoglobm

WIth 0")'9$l (~_ NoIe the sigmoIdsho~: it is relolive/yRot when P01 's >

80 mmHg flO 6lPa) but sleep whoM Po, foils below60 mmHg fS lPo)

Key point

When Hb approaches maximal O2 saturalion, furth~rincrealles in

Paz uu not significantly increase blood O! cuntent

"

PUlMONARY GAS EXCHANGE: THE BASICS

AlVEOUR Vllffll.ATlON AND ~

We hav*, nowseen. how P«>z re,;;uJa~ the ~. But what dcl'erlniJ'w><l

P«>z'

There are three major factors that dictate the Pac,;:

1, Alveolar ventilation

2. Matching of ventilation with ~rfusion(VIQ)

3. ConCUltntion ot 01 in inspired air (FiOa)

Alveolar ••ntilation

O:z moves rapidly from alveoli to till: bloodstream - so lhehIgher thr uluwwrPo" Ihe hixhtr the PIlOz·

Unlikp air in the atmosphere, alveolar air rontain.'l significant

amounts of CO:z (Figure 6) More CO:! means a lower p~ (remember

An mcreaseinalvoo1acventilation allows more CO:z to be 'blownoH',

resulting in a ~ alVl."'Olar ~. If,on the otherhand, vcntilatiorl.declines L~accumulate; at thecxpenw of O:z and alveolar ~

falls

Whereas hyperventiation can mcrea!le alveolar pO:!only slightly

(bringing itcloser to the Po:zof inspin>d air), there is no limit to howtar alveolar f'oz (and hence P~can fall with inadequate v.:ntilation

12

PULMONARY GAS EXCHANGE: THE BASteS

Both uxygen.ation and COl elimination depend on alveol.u

ventil.ation: impail'e'd vcntiJiiltion cau5e5 PliO, to fall and Plica, tu

ri,

13

PUlMONARY GAS EXCHANGE: THE BASK:S

Ventilation/perfusion mismott:h and fhunring

Not all blood flowing thmugh the lung meets wt>U-venhlat~alveoli:md not all vt:ntilatcd alveoli ilrt' pt'rfused with blood - E"Speeially Ultht> prest>ncp of lung disc~.This problem is known as ventilationI

perfusion (V/Q) mi'lmatch

lmagmeifalveoli in one area of lung arepuorly venbJittPd (e.g duc

tocollapse or consolidation) Blood pitssmg thot' alveoli n>tum.~tothe arterial circulation With Ie::;:;0, and more('01 than normal This

is knuwn as shunting l

Now, hy hyperventilnting. we canshiftmore air in and out of our

remaining 'good alveoli' nUs allows them to blow-uff eXlra C~ SOthat the blood passing ttwm can offload more CU:!.'The luwer Co,

in non-shuntrtl blood compertSittH fOf" the higher COl in huntedblood, m;untaming tht! poleD,

The :,ame docs NOT apply to uxygt!J\i1lion Blood passing 'good

alveoli' isnot able to carry more0, Mause ils hM>moglobin i::

alrt>itdy maximally :xIturatcd \,nth <-1:1 (remember: flat part of curvt:,

page 11) Thf' non·shunt~blood lhenofoN' carumt rompensah> for the

low O:z levels inshuntt"d blood and the p~ falle;

Key point

V/Q mismatch allows poorly ol()'genated blood tu re-cnter the

arteriill circulation, thull low~ring Pao" and Sao2"

does not I~ad to an inC~ilse in PacOr

'Tl\(> tPTITIalso appliestobluud lh"t bypasses alveoli altogelher(anatomICal

~'W1IUlg)

14

PULMONARY GAS EXCHANGE: THE BASIC",S, _

PUlMONARY GAS ~CHANGE. mr BASICS

The fraction of inspired oxygen (FiO:J refers to the percentage of

0:m the air we breatheIn. The FiOz in room air IS 21%, bul can "*increast"d wIth supplementaJ~.

Aluw PacJ.z may result from t'ithcr VIQ mismatl :h or inadequate

vrnblabon and, in bothca~,increusi.njl, the F~ willimprove the

PaOz. 'l~ ~)(act r~ rcquirem nt vane!:> depending nn how severely

device (figure 8) When thf' cause is inadequate ventilation it must

be remE>mbered that incrc3Sing riO, wIll not rev~the rise in P~.Supplemental~ makes ABC analysis more complex as it can bedifficult to Judgc whether the P/Kh is appropriately high for th~

F~and, hE"llet", whl.>thcroxygt"nabon lS impaired A useful rule otthumb is that thp diffeft'J)(.'C betwffn r~and POOl (in kPa) shouldnot normally be ~r~aterthan 10 Howevpr there isoften a d€'gree

of uncertamty as to !he pl"€'CiseFiO,. and, ifsubtle impaU"lucol is

suspected,thf' ABC should be ~ atedon room air

OXYgMI et.livery devic.,

NasolfNO"gt. f~ < ~ ComfOl'tol:h ond comenient FiO,

n0n-specific: depends on flaw rem t1-6 Vmin) and venhlabon

Stondard fm;" mask: fiO, 30-50% at flow rotel6-10 Vmln bul

ImpuKise Mot COllie CO:! relention ot flow, < 5 Vmin ('rebreolhing') 100

not 1IJefu1 Jar providing 10- ft0:2

fixH p«fOiilNilKe (high&wl ~ rno~ F~ 24 00% Ddivers fUced,

prediclabl Fi02• Ideol for providing controlled, occurote O:z therapyallow

CorN;ef\lfQl;QI1S

foe. meuk wiIh re••nooi. ft0:2 6IJ 8O".li Con ochie¥e _ higher

fiO:z with IighHifhng rnosJc Useful for ano.llefm UM in respiratory

emergencIes

fndotracheGl intubation: fi0221-100% Uled In soyerely un 11

potierlb with very high ~ requiremenls, especioMy wifh venhlolory!oillire

Patient issedoltid ond InlI<::hookollyventiloted

,.

PULMONAAY GAS EXCHANGE: THE BA5K.:S

Fbledpelb Ifs milt:

VaoobIc perforrnarx:emask

Figun a Oxygen deJ,WKY clevius,

17

Hypoxia refer.; tuany stld~;11 whIch tissUt'S M:'riot lI1I iruzdeqlUlksupply

of01to support nOrmQIlJt7'Obic mrl/lbolism l (Figwe9) It may result

from either hypoxl!emia (!lee below) or impaired blood supply to

tis~ues (isl.:hacmia). It is ('Iften associated with lactic acidosis as cells

resort to anaerobic metabolism

Hypoxa~mlarefers to tmy slQf~ in wIridr 1M O2rontent ofQrlmal blood

haemoglobin (anaemia) Of reducw affutity of ha~mog1obinfor Oz

(e_g carbon monoxide).

Imp.tired oxygr:nation refers to hyporMmJII fC>.41tingJrom rtduaJ.

tnlmferof D1from lungs to thebloodstrtflm. It isidentified by alow P/Kl:!,

« 10.7 kPa; < 80 rnmHg).

It is important 10 note Ihc distinction betWt:'ell impaired oxygenation

(which results in hypoxaemia) and IrwdLqllllteoxygcnation (whkh

re;ults in hypoxia) Constder a palimt with a PlIU:! of 85 kPa He M 'l

impaIred oxygenation suggesting the prcsmce of irnportanllung

diSE'OlSf' NeveI"lhtllt.-ss, hisPao.z would usually result in an ~ > 90%

and, protlidt'd th£ haemoglobin and (llrdiac output are normQl, adequate

0:l: delivery to tiS$Uell.

lit" often m.lvisabl(' to u.'\t! the term 'm "uc hypoxia' to avoid any l't>nfusion.

11

rnsoRDERS OF GAS EXCHANGt:

HoomogIobil low/1QernagIObi'I low~

I.WlIlbIe 10 carry ~ (~) (1IIp"oed

••

DI~DERS OF GAS EXCHANGE

TYPE 1 RESPIRATORY IMPAIRMENT

Typt! 1 respiratory impairment' is defined as low P~with norum!

or low P~.This implies defective oxygelation despite adequateventilation V,Q mismatch isusually responsibl4" and may tc5ult

from ;1 numbt"r of causes (Box 1.3.1).The PIIJCO.z is often low due tocompt!J1satory hyperventilation

If the ABG is drawn from a patient on supplM'lf>tltal Oz. the Pl7O-z maynot bebelow the normal rangt", but willbeinappropnately low forthe FiO,.

The Sf>verity of type 1 respiratory impainnent i~ judgt 'l:1 according

to the scale of~ resulting hypoxaemiol and, ultimately, the

presence ofhypoxia (fable 13.1) Hpre it IS important to rernmilicrthe 0,.dissociation curve Reductions in PtIOJ as far as 8 kJ'a have

a relatively minor effect on Sao:zand are well tolerat~. Beyond

this threshold, we reach th£' 'steep part' of lh£' curv£' and further

reductions in PtIOJ will lead 10 much greater falls in ~ significantlylowt'ring the ~content ofarterial blood

Initial treabm ll of type'1 resplJatvry impairment is a~ at

achieVing an adequate Pac; and Sat~ Witll supplemf'ntal O2whileatlcmpting to COIn:dUte W\derlying cause In many ca5f'1l pube

Olomt'try canbe used as an alternativE' 10 repeated Aac; sarnplmg tomonItor progress

'We USl' thf lftm 'inlpairu-."ll' ralMrthan 'fai.lure' hL-rc as t~diaSJ'OSlS 01re5pU"ilkw)' failUT# requires I Pao:z < 8 kPa « 60rnmIiX)

DISORDERS Of GAS EXCHANGE

So;.: 1.3.1 Common CQU5e'5 of~ 1 respUoIwy lmpai ent·~

Chronic OO'l'U<:llve pulmonary diseose

Table 1.3.1 Auesdng MYerity of type 1 respiratory

at" _ken of e intpo t

• H'9h f~ reqoJiremenl$ to maintain odeqvole Paa,

• loctic: ocidl)$i$ lindicOling tissue hypolliol

• Orgot'! dysfunction (drOWSlnen. confulion, reool fo,luf., hoemodynamlCcoIIopMl como]

21

DISORDERSOf GAS EXCHANGE

TYPE 2 RUPIRATORYIMPAIRMENT

TYJX' 2 respiroltOry impairment is defined by a high PoX U:l:

(hypercapma) and is due to madequate alveolar ventilation Sinceoxygenation alw depends on wntilation, the Paut is usually low, butmay be oorffial if th pabenl is on 'iUpplemcnlal 07' It is important

10notp that any cause of typt! I impairment lllay lpad to type 2

impairment ifexhaustion s\lpervencs

Arnte rises in Parll:! lead to dangpmus accumulation of add in theblood (see ~'Clion].4) and must be rf'\·er~:tJ. Chronic hypercapma l:>olccompamed by a rise in bicarbonate (HCO~),which pr~rvcsaCid-base balancp Howcwr, p"tiPTlts with chJ'()r'lic type 2 irnpaUID\.'n1who expcrienn> a further sharp decline in ventilation will also holYC

a rapid rise in PaC02 tacute Oil chronic),le~dingto aCid I.ccum\llation.md low blood pH (Table 1.3.2)

Supplemental ()2 improves hypoxaemiJ; bUI nol hypercapma, ~

trf'atment oftype 2 ft>Spuulory impainncnl should also include

measures to improw \'ffitilation (e_g. w.ersal ofsedation, reJjpf

of airway" ~Iruclion,a';si"tetJ ventilation) Thc OVPrzealous

lldTlunistration of supplemental0,.to som!' patients with chnmic ty'pf'

2 impainnent may furthcrdep~'iventilation by abolishing hypoxicdrin> (p 7)

Pulse oximetry provides no mfurmation on PIICOzso is nut a suitahlesub:.tilutC' for ABC monitoring in tyJXl: 2 ~uatory impairment

22

OIS<:)iOERS Of GAS EXCHANGE

Tobie 1.3.2 The ABG in dfff .t pullern, oftype 2

Bolt.1.3.2 ~I1'l~(QUMS of ~ 2 reJPiratory.lmpoirment

ChronicO&tTur;tive pufmonory di*Jse"

-Drowsiness

Bounding pulseHeodoche

.3

DISORDERS OF GAS EXCHANGe

HYPERVENTILAnON

Hypervl'!nlliation leads 10a low Pan> > (hypocapnia) and a

corre:por.ding ri~ in bluud pH (set> Sfftion lA). Inchrot"Jc cases

it is accompanied by a ri'it" in HC0.J, which corrects blood pH AnincreaSf" in the ratl: olnd depth of breathi.ng isusually apparent Alarge drop;n Pan" may lC<ld to tingling arowld the mouth dod

extrt'llutics, light·hPadedne.s ilIld even 'lyncopc

Psychogeruchy~rvcntilationoften presents in a dram.tlic fashion,with patients complaining of severe breatWcssness and an inability

tu tuke in enough air It may be difficult to distinguish from

re>piratory disc<lse Tht>ABC J>hows a low PIILUz with a normal p~

H)'peJVenhlahon abooccurs a5 a compensatory response to

m~tabolic acidosis (secondMy hYP*'rvpnhlation), as dE"lCribed in

section 1.4.OthercaUS('5 are :ihown in Table 1.3.3

Solicylote lollicity HepatICcirrhosis

-DISORDeRS Of GAS EXCHANGE

SUMMARY Of GAS EXCHANGE ABNORMALITIES

T'ht> four lllai.n putt~rns of ABC abnormality in disorders of gas

exchange are summarised in Tuble 13.4

Tabte 1.3.4

I t 'espualOl"f •'"'PO*" nt

°Acvle on dlfonk; di.lingui~Fromdwonic bv pre ,roc 011 H'

A note on ••• the A-a gradient

The A-o gradient i$1hc diK.rencll bet ee" the alveolar fIt? love<aged

ocrou01 ~l ond fie ~ in or1efiol b'ood. It tells I,IS wheIher the Pao,

is oppropriole for the level of alvcolar veolilation end is Ihen~for a meo~ure

01 the degree of VjQ mismolch.

In proclice its moin \I$OS lie in detecting subtle IncreaSti in V/Qmlsmoteh

wiler h ~ I~ WIll willlin the normal ronge !e.g. puknonoryemboli,",'

ond ideotilying the presence of V/Q milmalch in patients with Iypfl

2rc$puafory impairment {thi~ distlnguiws pure Iype 2 respiratory

Impairment from mi:wd type I ond type 2 Impairmentl

lIlllbook but, for !hole inlafel<led, a guide can be lovnd in Appendix 1

ACID-BASE BALANCE:

THE BASICS

The terms aridity and alkalinity simply refer to the «()JlreIl.tration

of free hydfoR,en ions (H') in II solution H' concentration can be

~xp~.Jwro:l1y in nanomoles per litre (nmol/L) or as pi I

(s-over)

Solutions with hIgh W (low pH) are acidic and those with low

H' (h.igh pH) are alkalinf' The POint ilt which a substance changes

from alkah to acid is lhc neutral point (pH :z 7, H' s 100 nnwl/ L).

An i'ldd is a 'iubstance lhat ,dea5f!S H' when It l~ dissolved in

~lution Acids ttwrefotf" increase ~ H' concentration of the

solutiun (lower the pH) A base i.~ a sub:.tancc lh.'\1 a«tpt.'1 H· when dis.c;olved III solution R"lSeS therefore lower the H' concentration

of a solution (raUlt! the pH) A buIll?( is a substance that can either

;lea-pI or releilSt> H' dependillJ!!; on the surrounding H' concentration Buffers lhcrdon> rl'Sist big changt:lll in H' concentration.

Human blood normally h.\5 a pll of 7.35-7.45

(II' _ 3 ~.5 nmol/L) so is ::o1ightly alkalinE' If blood pH is below the normal ranFje « 7.3 '), there IS an addacmia If it is above the normal range (> 7.45), there is an alkalaemia.

An acidosll'l " any pnx:ess thallow~blood pH whereas an alkalosIS

is any pt'ClCeS6 that r3lSeS blood pH.

2'

AClD-aASE BAlANCE: THE 8ASICS

What as pH?

ThepH (power 01 hydroget'l) Kale l~ a ~Implln.d 'W'a'f ofexpreuing large

~ in H' =ncerflluhoo, though ifyou' notcorne ouou jf before you

might think II 'NO$ d.t.iglMd iuu to confu~ you!

It i$ a MgUtive logarithmic KoIc fFigvfe 101. The 'negative' meon$!hut pH

~ get lower as !he H' concentration increoMli flO a pH 01 7 1 ;$ moreOCIdic thon 7.21 The 'Iogarilhmic.' meons thol a Mlift in pH by one numbel r.prelents a 10-f01d chonge in H' concenlfolron (so 7 Ii 10 times more

ocidic than B)

Why i. aci~s.bolance important?

J;or cellular pI"0CCSS4.'S to occur effiCIently Ihf II' concentration lJ\USl

be kcpl within tight limit!! Failure to maintain pH baJarn "C Ical.!s 10

lIlefficient cellular reactions and ultimately death (FigurelO)

, pHM """

27

ACID-BASE BAl.ANCe THE BASICS

MAINTAINING 4CID-8ASE BALANCE

What generates H+ ions in our bodies?

n.e breakdown of fats and SUgMS for energy generates ~ which,when dis:dvro Inblood, fOf"DlS carbonic acid (see Box on page 211).

M~abolism of pmtPin produces hydrochJonc, :lulphurit: and otherso-called 'metabolic acids'

H· ions mu.st, therefore, be rcmovL'd to maintain normal blood pi!

What removes H+ ion from aur badies7

Respiratory mechanisms

Our lungs are responsibl~for removillK CO2_P'ICO:!, the parti ,1

pressure of carbon dioxidt> in our blood, is determinoo by alvL'Olar vCl1tllo:ation. IfC~production is altt"red, we adjust our breathing

10exhale more or k'SS COgas IlI.'."CSSary 10maintain PlIC'O;z withinoormallimifs Thebulk of the acid prodlK.L'd by our bOO.ies is in the

form of COz, soit is our lungsthat excrete the vast majority ofthe

o:aud load.

Renal (mefobollc) mechanisms

The kidneys art' r(>$poru;ible for eXcrelmg rnmbolic acids. TIleY

~'l,;rctc H' ions inio urint> and reabsorb HC0.'l from urine HCo,io:t a

base (and therduA:' <1<.:CCPlS H' ions), so it reduct'S the ("onr('ntration

of H· ions in blood The kidn~yscan adjust urinary H' and IlCo,excretion in responSE' to changes in metabolic led pnxluL1ion

ACID-BASE BAl ANC~: THE BASICS

MAINTAINING ACID-BASE BALANCE

The l'Cnal and respiratory syst ms operat", Jomtly to maintain blood

pI-{within normallirruts Ifonesystem IS ovtrWhelmcd, leading:

toa ch;mge in blood pi I, theotl'llo'[ usually ddjUSl$, automatically,

to limillhe dlSturh;mce (e.g Ifkidneys fail to ~cretp m~abolk

acids, ventilation is UKTlo'a 'led to exhale mure C00 This is known all

wlilf!t-1ISQUm/

Importantly, lvrnpensatOry change1l in respiration haprt"" over

minulesto hours, wherc<li:> mt>taoolic rcspou!>eS tak(> days to develop

Jwt one equation•••

~ -This one eqoolion is c:rucial to understanding ocid-ba.se bolonc:.;

~o + CO2+-+ ""Cal H' + He0s

Firs/ly It show51hot C~, when dissolved In blood, becon'lfts on <rid_

The mOle COz added 10 blood, the more H1CO, lcorbonic oc,dl is

produced, wIloch dissociatesto release free W ions

S8ct:Jldy, it Pfedicts Ihot blood pH depends not on the obsolut.t ornoonts

orCo,;01 HCOl present but on 1M 'Otioof CO 210 HCo.,- Thus, (] change

in C~ will not Ieod to a c:horoge in pH if III, boIonced by 0 c:honge in

HC~!hot p'esetvei Ihe ratio (and vice nal· Since C~ is c:ontrolled byrespirolion ond HeO, by renol~, !his expkJlnl howcornpensotooncon pr~t c:honges in blood pH

29

AClD BASE BALANCE: THE BASICS

DISrURBANCES OF ACID-BASE BA~LANCE""

An acidOl'iis is any process that acts to lower blood pJ I II it is due to

;; lise in P~0z.itis calied a r£~pirator.LJ acidosis; jf it isdue to any other

C<lUSC, then HC03 is redw.:oo and it is called a metabolic ucidosis.

An alkalosis is any process that acts to increase blood pH If it is nue

to a fall in PQ~, it is called a respiratory alkalosis; if it is due to anyother cause, then HC03 is raised and it is callt -d a metabolic alkalosis.

• Metobolic olkolmi~

_ Metabolic:: ac::ldalisAdd-hase disturbances can he considered as a set of scales

Normol acid-bose balance

Wht "11 i1cid base billance is entirely normal, with no alkalotic or

acidotic pressures, it is like haVing a set of scales with no weights on

it (Figure 11)

Uncompensated acid-base disturbance

VVhen an acidosis or alkalosis deve.lops, the scales become

unbalanC'f'd, leading to acidaemia or alkalaemia respectively

in Figure 121herc is a primary respiratory acidosis with no opposing

metabolic process

3.

ACID aASE BALANCE: THE BASICS

AClD-8ASE BALANCE· THE BASICS

COMPENSATED ACID-BASE DISTURBANCE

As described earlier, a respiratory or metabolic disturbanre is often

C9",;>rll5(llro for by i'ldjuslmMt of the utl~system to offsf1' the

primary Jisturbiln :c

Figures 13 and 14 represent two St.'Cnarios in which the hU1~have

responded to a primary metabolJc aad~isby increasing alveolarventilahon to chminalC more CO2 (compensatory respiratory

aJkillo<;i<;,) In Figure 13 an acidaemia pE'rsic;ts despite u.IInpcns;!tion

(partial compmsation); In Figure 14, blood I'll has rrtumed tu the

norm.u r.lngc (full cOffipens;ttion)

Whpn facffi with ~uchlUli\BC, how can wp tell wru<:h iSlhe primarydisturbance and which is t~ rompcnsalOry pf'OCt"<lS?

The fir.,t rule 10 remember is that llwJcumprnSlltion dots not(ICCIlr.

The midpOint of the acid basc scales liesat a pH of 7.4 (H' 40) If

the scales tip loward ilCIdaemla (pH <7.4), this <;,uggests a primary

acit.lotk process, it they tip mward alkalacmia (I'll> 7.4), a primary

alkalotic pruc(,::>s is likely

The 5('('ond rule 15 that thepatirnt is /IIQre imporltlnlthnn lhe ABC.

When considering an ABG, one must always lake acrount ofthe

clinical ('\.IIltexl For exampw,if the pabent in Figure 14 W~ diabetic,with hIgh levt>ls of lc.ctoncsin the unne, It would be obvious thai Ih

melabolic acid~lswas a primary pJ"O("~(diabetic ketuadJosis)

It ;$ not ~ «)$Y kl ~ two pnmoryoppoo$Ong p«X:flM$ from

a «WTlperuoted d,w.bonce ; more pr«:iMl method Ihon !hotde~

obo involvM cakvlating Ihe ellpoc.oo compensatory response lor

ony g,ven primary di1turbonce Howevtlr the~ colculations are usually

unneceuaryond ale not required for the case ~r~ in Pan 2

ACID-BASE BALANCE: THE BASICS

,

ACID-BASE BALANCE: THE BASICS

MIXED ACID-SASt DISTUIlBANCt

When d primary re.piratory disturbance and primary metabolic

di<:turbance occur simultaneously tht.-re IS :.aid to be a minoJ

acid base disturbanct'_

Ifthoe two pnx:t.~~oppose each other the patternwill bE'simiiartoa compensated aCld-base dlsturoanre (FigUl\: 14) and the resultin~

pll d('ran~ementwill be minimised A good@xample c salicylat~

poisoning where primary hypeiVentilation (respiratory alkaIMl<:)and metabolic acido:.lS (~hl:ylilte is acidic) occur independently

On the other hand, if the two processes call~pH to movt: In tht:

sall1~ diro;:tioll (metabolic acidosis and rl:'Spiriltory addos! :: or

metabolic alkaloMs and reo.piral.ory alk.1.1osis), 1 profound acidaentia

or alkalaemia may N"iult (Figure 15)

The nomogram

An alternative way to analyse ABG~ ~ to usc the acid base

nomogram (Figu~16) Ky plotting the PIK.u,and H· /pH valut.'S unthcABG IlOJll~ram.most ADGs can hoe analy<;ed Ifthe plotted pomtlleO oubide tilt:dt.'Sigfl.ltl '<l areas, this implies a mixed disturbance

ACID-8ASE BALANCE: THE BASICS

DISORDERS OF

ACID-BASE BALANCE

METABOLIC ACIDOSIS

A metabolic addosis is any pl'Ol "CSS, otlu:r tlum a rise i1l p~ thai actl

10 lower blood pH It may occur through accumulation of ffiE'tabolic

.:lcid~ (excess mgeshon, 1nrrf'.1"oed production or n>duced renal

excretIOn) or through exct'SSi"'e loss of base (HC~).c.l1culaling theanion gap (sec over) may help to ~tab~hthe caU1Ie uf a metabolic

acidosis.

Metabolic aridOf;is is recognised on an AI}(; by low HCo,

(and negative bas<' exC('5S (BE» TIlcre is normally a rom~tury

increase in aly\.'OI.tr vt!1\b1ahun to lower l'at.:0:!. If resprratory

com~bonIS overwhelmed, an acidaf'mia will result ~.~ty

must be judged aN'ording to both thto lmderlying process and the resulhng acidat'mia An J ICO;, < 15 mmol/L (or BE < 10) indiCi1t~

a severe acidotic process whereas pH < 7.25 (H~:> 55) constitutes serious at.idaenua.

The dominant symptom in metabolic acidosis is often

hyJX"f"entilation (Kussmaul's respiration) owing to the re.piratory compcnsatiun Otht:r ~Ignsare fairly non-speafic or related to thf'

wu.lerlying cau~ Pmfound acid:u>mia (pH < 7.15; I'· > 70) may lead

to arculal0'1' shod:, ~ dysfuncLion, and, uILimatcly death.

Specific caU$CS or mdabolic aadlY.>1S are chscussed in greater detail ill

the relevant Casel in Part 2.

36